Evidence map›Paper›PMID 29200203›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2018

miR-200b/c attenuates lipopolysaccharide-induced early pulmonary fibrosis by targeting ZEB1/2 via p38 MAPK and TGF-β/smad3 signaling pathways.

Yongmei Cao, Yujing Liu, Feng Ping, Lyu Yi, Zhen Zeng, Yingchuan Li

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Article in Laboratory investigation; a journal of technical methods and pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed.

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  20. Lung Cancer Models Reveal Severe Acute Respiratory Syndrome Coronavirus 2-Induced Epithelial-to-Mesenchymal Transition Contributes to Coronavirus Disease 2019 Pathophysiology.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Yongmei CaoDepartment of Critical Care Medicine, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, China.
Yujing LiuDepartment of Critical Care Medicine, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, China.
Feng PingDepartment of Critical Care Medicine, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, China.
Lyu YiDepartment of Critical Care Medicine, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, China.
Zhen ZengDepartment of Critical Care Medicine, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, China.
Yingchuan LiDepartment of Critical Care Medicine, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis triggered during the early stage of acute respiratory distress syndrome (ARDS) contributes to poor prognosis in patients. However, whether microRNAs (miRNAs) can serve as therapeutic targets for early pulmonary fibrosis during ARDS is still largely unknown. In this study, we evaluated the effects and mechanisms of miR-200s and its targets ZEB1/2 in lung tissue. An early pulmonary fibrosis mouse model caused by ARDS was established via a lipopolysaccharide (LPS) three-hit regimen. Lentiviral packaged miR-200b/c cDNA or ZEB1/2 shRNA was intratracheally administered into the lungs of C57BL/6 mice 1 day before an LPS injection was administered. In vitro, following a 30-min pretreatment with miR-200b/c or SB203580/SIS3, RLE-6TN cells were stimulated by LPS or LPS + transforming growth factor-β (TGF-β) for 24 h. miR-200b/c and E-cadherin protein expression declined, whereas ZEB1/2 mRNA and protein and vimentin and α-smooth muscle actin (α-SMA) protein levels gradually increased during the development of pulmonary fibrosis. Furthermore, both the overexpression of miR-200b/c and the silencing of ZEB1/2 significantly alleviated pulmonary inflammation and fibrosis, reduced vimentin and α-SMA expression, and increased E-cadherin protein levels. In RLE-6TN cells, LPS combined with TGF-β exerts synergistic effects of increasing vimentin and α-SMA protein levels, increasing p38 and smad3 phosphorylation and reducing E-cadherin protein levels, which were reversed by pretreatment with miR-200b/c or SB203580/SIS3. Our findings demonstrate that miR-200b/c was downregulated, whereas ZEB1/2 was upregulated in the development of LPS-induced early pulmonary fibrosis. miR-200b/c exerts a protective effect by targeting ZEB1/2, which may be associated with the inhibition of p38 MAPK and TGF-β /smad3 signaling pathways.

Indexed as

MAP Kinase Signaling SystemActinsAnimalsBronchoalveolar Lavage FluidCadherinsCell LineDisease Models, AnimalEpithelial-Mesenchymal TransitionLipopolysaccharidesLungMice, Inbred C57BLMicroRNAsPulmonary FibrosisRandom AllocationRatsRespiratory Distress SyndromeActinsalpha-smooth muscle actin, mouseCadherinsLipopolysaccharidesMicroRNAsMirn200 microRNA, mouseRNA, Small InterferingSmad3 ProteinSmad3 protein, mouseTransforming Growth Factor betaVimentinZEB1 protein, mouseZEB2 protein, mouseZinc Finger E-box-Binding Homeobox 1Zinc Finger E-box Binding Homeobox 2

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.